How Do I Love Thee Sugar?

SugarInFlames The idea that there is a relationship between inflammation and disease is not new. In recent times, sugar consumption has been blamed. But sugar is highly anti-inflammatory. Let me count the ways.

For thyroid energy system metabolism to function properly, sugar is required, and so the body will make sugar available whether you eat it or not. Sugar is important to the depth and breadth and height that energy can reach. Unfortunately, not all the ways are made equal.

Interference with energy metabolism and a lack of sugar availability, have a lot in common. Both can cause an increase in stress hormone levels, two of which are adrenaline and cortisol. Both can also promote greater release of free fatty acids out of storage as alternative fuel.

Free fatty acids, by interfering with metabolic function, can promote stress and inflammation. If fat released from storage is composed of large amounts of polyunsaturated fats (PUFAs), interference with thyroid systems and metabolism is more severe, and can become chronic. PUFAs are directly highly inflammatory, and sugar protects against free fatty acid release.

Rising levels of the catabolic stress hormones such as cortisol and adrenaline, promote the release of PUFAs out of storage, as well as the breakdown of muscle and other tissue, and the increased circulation of potentially inflammatory amino acids, interfering with blood sugar regulation, and encouraging inflammation. Sugar lowers adrenaline and cortisol levels.

When thyroid energy metabolism is under functioning, resting body temperature tends to be lowered and digestion is inhibited, and this often leads to an overgrowth of bacteria in the intestines, and a subsequent increase in endotoxin secretion. Mild hypothermia has been shown to cause inflammation and bacterial endotoxin is directly inflammatory. Sugar, via the promotion of thyroid function, improves body temperature regulation and digestion, and protects against endotoxin.

Endotoxin irritates the intestine, causing a rise in the release of serotonin and nitric oxide, both of which are anti-metabolic, and lead to an increase in the release of PUFAs and interference with intestinal barrier function. This allows for more of the inflammatory things to pass through to the liver and into circulation in the main system. Nitric oxide and serotonin are themselves inflammatory.

Excess endotoxin places stress on the liver, and interference with the liver slows thyroid function. Sugar fuels the liver, and increases the ability of the liver to deal with endotoxin and other harmful substances. When the liver is overloaded, more endotoxin can pass through into the main system, encouraging systemic inflammatory issues. An under functioning digestive system and liver, allows for a buildup of many stress related substances, including nitric oxide, serotonin and estrogen. Sugar protects against all these things.

Sugar helps with the production of cholesterol (an anti-inflammatory substance), and with the conversion of cholesterol into the highly protective and inflammation reducing hormones, including pregnenolone and progesterone. Cholesterol also protects against increasing levels of endotoxin and other toxins.

Pregnenolone and progesterone protect against stress and estrogen dominance. Excess estrogen is anti-metabolic, inflammatory, and an important promoter of stress and degenerative disease. The breakdown products of the PUFAs damage cholesterol, interfere with thyroid metabolism and liver function, and promote the accumulation of the inflammatory hormones and other pro-inflammation substances.

It’s hard to imagine many things being more inflammatory than the avoidance of sugar, especially under conditions of stress and inflammation, and under circumstances where the food supply has been compromised with the inclusion of all sorts of toxic and harmful ingredients, in particular high levels of the PUFAs.

The above combination of stress promoting (metabolism interfering) factors, can create a vicious circle type of scenario, leading to increasing stress hormone exposure, gradually reduced metabolic performance, and the promotion of a state of chronic inflammation and eventually disease.

One way to break this cycle, is to provide the sugar (and other things) required to reduce stress hormones, fuel energy system metabolism, digestion and liver function, improving protection against exposure to the inflammatory PUFAs, endotoxin and other anti-metabolic biochemical substances.

Excess sugar, whenever it gets converted into fats, is converted into the saturated and omega 9 fats, and both of these kinds of fats have protective and anti-inflammatory effects.

A diet avoiding the PUFAs, with plenty of milk, cheese, easily digestible sweet ripe fruits, and honey and sugar, is one logical and biologically valid approach, to protecting against exposure to ongoing and increasing amounts of inflammation.

I love thee sugar to the level of every day’s most metabolic need, by sun and candle-light.

If you like what I have to say, and you want more information (including lots of studies), showing ways that sugar protects against inflammation and promotes healthy metabolic function and blood sugar regulation, please check out some of my other articles, including Blood Sugar Beliefs and Do You Really Know It’s True? And please share this and sign the email list up top.

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Mild hypothermia promotes pro-inflammatory cytokine production in monocytes.

Manipulation of the acute inflammatory response by dietary polyunsaturated fatty acid modulation.

Acute induction of anomalous and amyloidogenic blood clotting by molecular amplification of highly substoichiometric levels of bacterial lipopolysaccharide

Study on Subclinical Hypothyroidism and its Association with Various Inflammatory Markers

Proinflammatory Effects of Hypoglycemia in Humans With or Without Diabetes

Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.

The Association of Cysteine with Obesity, Inflammatory Cytokines and Insulin Resistance in Hispanic Children and Adolescents

Subclinical hypothyroidism is linked to micro-inflammation and predicts death in continuous ambulatory peritoneal dialysis

So depression is an inflammatory disease, but where does the inflammation come from?

Methionine restriction on oxidative stress and immune response in dss-induced colitis mice.

Nitric Oxide and Major Depressive Disorder: Pathophysiology and Treatment Implications.

Human Monocytes Engage an Alternative Inflammasome Pathway

Neural response to emotional stimuli during experimental human endotoxemia.

Associations of salivary cortisol levels with inflammatory markers: the Multi-Ethnic Study of Atherosclerosis

Association between hypothyroidism and small intestinal bacterial overgrowth.

Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice

Thyroid Hormones, Oxidative Stress, and Inflammation

Serotonin, inflammation, and IBS: fitting the jigsaw together?

Causes and consequences of low grade endotoxemia and inflammatory diseases.

Association between hypothyroidism and small intestinal bacterial overgrowth.

The impact of dietary methionine restriction on biomarkers of metabolic health.

The Contribution of Gut-Derived Endotoxins to Liver Injury

Mild hypothermia promotes pro-inflammatory cytokine production in monocytes.

High Fat Diet Alters Lactation Outcomes: Possible Involvement of Inflammatory and Serotonergic Pathways


Image: Tattoodonkey
Artist: Unknown

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